With New York still in the grips of a bed bug epidemic, the question keeps popping up: why are these little bastards so damned hard to kill? According to new research, their resurgence in the last few years has definitely been closely linked to the Big Apple, but it's actually been happening in all 50 states. The infestation is the worst since the 50s — and the bugs have developed a resistance to pyrethroids, one of the few types of insecticides used to do them in.

More specifically, bed bugs have a resistance to deltamethrin and beta-cyfluthrin, two of the more popular pyrethroids on the market, and the researchers have picked apart the genetics behind this development. They compared a resistant population of bugs to a non-resistant group that had been raised in labs since the 70s — the wild ones required 5,200 times more deltamethrin or 111 times more beta-cyfulthrin to kill.

The resistant bed bugs had multiple genetic defenses against the toxins. There are three specific genes (cytochrome P450 monooxygenases, carboxylesterases, and glutathione S-transferases) that can bind to, deactivate, and break down insecticides, and all three were cranked way up in the wild bed bugs. The pyrethroid also targets the insects sodium channel, which in response had mutated, making them partially resistant to the effects.

Ladies and gentlemen, the very definition of evolution. A constant pressure on the population in the form of a limited number of insecticides means that bed bugs with mutations that offer them a resistance are substantially more likely to live long enough to reproduce.

This means that there's a definite biomarker that separates the resistant insects from the rest. And hopefully, we can now engineer a smart pesticide which will actually succeed in killing the horrible things.